In normal scarring the newly deposited connective tissue matrix undergoes remodeling. In conditions of excessive scar formation, such as hypertrophic scar, there is little remodeling and immature collagen accumulates. We propose to find new ways to control scarring. 1. We have preliminary data showing that the procollagen peptidase which cleaves the carboxy terminus of procollagen is an ascorbic acid dependant enzyme. The further characterization of this enzyme may lead to the identity of a specific inhibitor. By blocking the conversion of procollagen to collagen, defective collagen fibers should form, such as those seen in dermatospaxis. These fibers should readily undergo turnover and remodeling. 2. We have found mature granulation tissue homogenates will disrupt the growth of young granulatign tissue. The isolation and characterization of the factor(s) responsible for this inhibition will be pursued. 3. Colchicine inhibits both collagen synthesis and open wound closure, but promotes the secretion of collagenase. With these three attributes it may be an effective pharmaceutical for the control of scar formation. Its effects in model wounds will be examined. 4) Zone Chromatography has revealed the presence of types A-B and IV collagens as well types I and III in normal and hypertrophic scar. The possibility that hypertrophic scars may have type II collagen will be investigated.